Human exposure to airborne carbon nanotubes (CNT) is increasing because of their applications in different sectors; therefore, they constitute a biological hazard. Consequently, developing studies on CNT toxicity become a necessity. CNTs can have different properties in term of length, size and charge. Here, we compared the cellular effect of multiwall (MWCNTs) and single wall CNTs (SWCNTs). MWCNTs consist of multiple layers of graphene, while SWCNTs are monolayers. The effects of MWCNTs and SWCNTs were evaluated by the water‐soluble tetrazolium salt cell proliferation assay on NR8383 cells, rat alveolar macrophage cell line (NR8383). After 24 hours of exposure, MWCNTs showed higher toxicity (50% inhibitory concentration [IC 50 ] = 3.2 cm 2 /cm 2 ) than SWCNTs (IC 50 = 44 cm 2 /cm 2 ). Only SWCNTs have induced NR8383 cells apoptosis as assayed by flow cytometry using the annexin V/IP staining test. The expression of genes involved in oxidative burst ( Ncf1 ), inflammation ( Nfκb , Tnf‐α , Il‐6 and Il‐1β ), mitochondrial damage ( Opa ) and apoptotic balance ( Pdcd4 , Bcl‐2 and Casp‐8 ) was determined. We found that MWCNT exposure predominantly induce inflammation, while SWCNTs induce apoptosis and impaired mitochondrial function. Our results clearly suggest that MWCNTs are ideal candidates for acute inflammation induction. In vivo studies are required to confirm this hypothesis. However, we conclude that toxicity of CNTs is dependent on their physical and chemical characteristics.

While new exciting applications arise from rapid development of new advanced materials, their lifecycle, from production, processing, to degradation or even combustion, may inevitably result in the release of particulate matter into the environment. [1-3] According to the Organisation for Economic Cooperation and Development (OECD) and the World Health Organization (WHO), inhalation of particulate matter, predominantly of anthropogenic origin, is associated with several million human deaths globally every year. [4-6] While larger particles, deposited in airways, can be efficiently cleared from the bronchial region by the mucociliary escalator, [7] nanomaterials, the term used here for both submicron-sized particles (at least two dimensions below 1 µm) and nanoparticles (at least one dimension below 100 nm), can reach the alveolar region. [7,8] Due to the persistency On a daily basis, people are exposed to a multitude of health-hazardous airborne particulate matter with notable deposition in the fragile alveolar region of the lungs. Hence, there is a great need for identification and prediction of material-associated diseases, currently hindered due to the lack of in-depth understanding of causal relationships, in particular between acute exposures and chronic symptoms. By applying advanced microscopies and omics to in vitro and in vivo systems, together with in silico molecular modeling, it is determined herein that the long-lasting response to a single exposure can originate from the interplay between the newly discovered nanomaterial quarantining and nanomaterial cycling between different lung cell types. This new insight finally allows prediction of the spectrum of lung inflammation associated with materials of interest using only in vitro measurements and in silico modeling, potentially relating outcomes to material properties for a large number of materials, and thus boosting safe-by-design-based material development. Because of its profound implications for animal-free predictive toxicology, this work paves the way to a more efficient and hazard-free introduction of numerous new advanced materials into our lives.